Serum Fas and Bcl-2 in patients with epilepsy
Objectives – The present study aimed to investigate the levels of the biochemical markers of apoptosis (soluble Fas and Bcl‐2) in the sera of children and adolescents with idiopathic epilepsy. Materials and methods – The study included 30 children and adolescents (mean age 8.03 ± 4.49 years) with...
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Veröffentlicht in: | Acta neurologica Scandinavica 2006-05, Vol.113 (5), p.315-321 |
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Sprache: | eng |
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Zusammenfassung: | Objectives – The present study aimed to investigate the levels of the biochemical markers of apoptosis (soluble Fas and Bcl‐2) in the sera of children and adolescents with idiopathic epilepsy.
Materials and methods – The study included 30 children and adolescents (mean age 8.03 ± 4.49 years) with idiopathic epilepsy, 16 of them were newly diagnosed, and 15 clinically healthy control subjects. Of the included patients, 22 had focal seizures and eight had generalized seizures. In addition to laboratory and radiological investigations needed for diagnosis and follow‐up, soluble Fas (s.Fas) and Bcl‐2 were assayed in sera of patients and controls by enzyme‐linked immunosorbent assay technique.
Results – Serum levels of s.Fas and Bcl‐2 were significantly higher in the patients group than in the control group; however, their levels were comparable in patients with different seizure types. Levels of s.Fas correlated positively with seizure severity and negatively with the duration from the last attack. Bcl‐2 levels were positively correlated to each of the duration of epilepsy, the severity of seizures and its frequency. There was a significant positive correlation between serum levels of s.Fas and that of Bcl‐2 and both were significantly increased in patients with uncontrolled epilepsy.
Conclusion – The present data demonstrate that markers of apoptosis, both the proapoptotic Fas and the anti‐apoptotic Bcl‐2, were proportionately elevated in sera of patients with idiopathic epilepsy, and their levels were related to the seizure severity and frequency. |
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ISSN: | 0001-6314 1600-0404 |
DOI: | 10.1111/j.1600-0404.2006.00592.x |